Chapter 049. Sexual Dysfunction (Part 3)

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Neurogenic Disorders that affect the sacral spinal cord or the autonomic fibers to the penis preclude nervous system relaxation of penile smooth muscle, thus leading to ED. In patients with spinal cord injury, the degree of ED depends on the completeness and level of the lesion. Patients with incomplete lesions or injuries to the upper part of the spinal cord are more likely to retain erectile capabilities than those with complete lesions or injuries to the lower part. Although 75% of patients with spinal cord injuries have some erectile capability, only 25% have erections sufficient for penetration. Other neurologic disorders...

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Chapter 049. Sexual Dysfunction (Part 3) Neurogenic Disorders that affect the sacral spinal cord or the autonomic fibers to the penis preclude nervous system relaxation of penile smooth muscle, thus leading to ED. In patients with spinal cord injury, the degree of ED depends on the completeness and level of the lesion. Patients with incomplete lesions or injuries to the upper part of the spinal cord are more likely to retain erectile capabilities than those with complete lesions or injuries to the lower part. Although 75% of patients with spinal cord injuries have some erectile capability, only 25% have erections sufficient for penetration. Other neurologic disorders commonly
associated with ED include multiple sclerosis and peripheral neuropathy. The latter is often due to either diabetes or alcoholism. Pelvic surgery may cause ED through disruption of the autonomic nerve supply. Endocrinologic Androgens increase libido, but their exact role in erectile function remains unclear. Individuals with castrate levels of testosterone can achieve erections from visual or sexual stimuli. Nonetheless, normal levels of testosterone appear to be important for erectile function, particularly in older males. Androgen replacement therapy can improve depressed erectile function when it is secondary to hypogonadism; however, it is not useful for ED when endogenous testosterone levels are normal. Increased prolactin may decrease libido by suppressing gonadotropin-releasing hormone (GnRH), and it also leads to decreased testosterone levels. Treatment of hyperprolactinemia with dopamine agonists can restore libido and testosterone. Diabetic ED occurs in 35–75% of men with diabetes mellitus. Pathologic mechanisms are primarily related to diabetes-associated vascular and neurologic complications. Diabetic macrovascular complications are mainly related to age, whereas microvascular complications correlate with the duration of diabetes and
the degree of glycemic control (Chap. 338). Individuals with diabetes also have reduced amounts of nitric oxide synthase in both endothelial and neural tissues. Psychogenic Two mechanisms contribute to the inhibition of erections in psychogenic ED. First, psychogenic stimuli to the sacral cord may inhibit reflexogenic responses, thereby blocking activation of vasodilator outflow to the penis. Second, excess sympathetic stimulation in an anxious man may increase penile smooth- muscle tone. The most common causes of psychogenic ED are performance anxiety, depression, relationship conflict, loss of attraction, sexual inhibition, conflicts over sexual preference, sexual abuse in childhood, and fear of pregnancy or sexually transmitted disease. Almost all patients with ED, even when it has a clear-cut organic basis, develop a psychogenic component as a reaction to ED. Medication-Related Medication-induced ED (Table 49-1) is estimated to occur in 25% of men seen in general medical outpatient clinics. Among the antihypertensive agents, the thiazide diuretics and beta blockers have been implicated most frequently. Calcium channel blockers and angiotensin-converting enzyme inhibitors are less frequently cited. These drugs may act directly at the corporal level (e.g., calcium channel blockers) or indirectly by reducing pelvic blood pressure, which is important in the development of penile rigidity. Α Adrenergic blockers are less
likely to cause ED. Estrogens, GnRH agonists, H2 antagonists, and spironolactone cause ED by suppressing gonadotropin production or by blocking androgen action. Antidepressant and antipsychotic agents—particularly neuroleptics, tricyclics, and SSRIs—are associated with erectile, ejaculatory, orgasmic, and sexual desire difficulties. Table 49-1 Drugs Associated with Erectile Dysfunction Classification Drugs Diuretics Thiazides Spironolactone Antihypertensives Calcium channel blockers Methyldopa Clonidine Reserpine β-Blockers
Guanethidine Cardiac/anti-hyperlipidemics Digoxin Gemfibrozil Clofibrate Antidepressants Selective serotonin reuptake inhibitors Tricyclic antidepressants Lithium Monoamine oxidase inhibitors Tranquilizers Butyrophenones Phenothiazines H2 antagonists Ranitidine Cimetidine
Hormones Progesterone Estrogens Corticosteroids GnRH agonists 5α-Reductase inhibitors Cyproterone acetate Cytotoxic agents Cyclophosphamide Methotrexate Roferon-A Anticholinergics Disopyramide Anticonvulsants Recreational Ethanol Cocaine
Marijuana Although many medications can cause ED, patients frequently have concomitant risk factors that confound the clinical picture. If there is a strong association between the institution of a drug and the onset of ED, alternative medications should be considered. Otherwise, it is often practical to treat the ED without attempting multiple changes in medications, as it may be difficult to establish a causal role for the drug.